Inhibition of salicylate on voltage-gated sodium channels in rat inferior colliculus neurons.
- Author:
Yanxing LIU
1
;
Xuepei LI
;
Hailin ZHANG
;
Yongli WANG
;
Hong LU
;
Xiang QI
;
Huijun ZHANG
Author Information
1. Department of Otorhinolaryngology, Peking University Third Hospital, Beijing, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Inferior Colliculi;
cytology;
Male;
Neurons;
drug effects;
metabolism;
Patch-Clamp Techniques;
Rats;
Rats, Wistar;
Sodium Channels;
drug effects;
metabolism;
Sodium Salicylate;
pharmacology
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2007;21(19):890-894
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the mechanism of the tinnitus inducer, sodium salicylate, on voltage-gated sodium channels.
METHOD:The effects of salicylate on voltage-gated sodium channels in freshly dissociated inferior colliculus neurons of rats were studied, using the whole-cell voltage clamp method.
RESULT:Salicylate blocked sodium current (INa) in concentration-dependent manner (0.1-10 mmol/L). The IC50 value for the blocking action of salicylate was 1.43 mmol/L. Salicylate did not affect the conductance-voltage curve and the steady-state activation curve of INa. The steady-state INa inactivation curve of INa was shifted by about 9 mV in the hyperpolarizing direction. In addition, salicylate delayed the sodium channel recovery from INa inactivation by increasing the slow time constant.
CONCLUSION:Our results suggest that salicylate causes a concentration-dependent blockade of INa and shifts the INa inactivation curve to more hyperpolarized potentials, which could be related to the mechanism of salicylate-induced tinnitus.